Expression Of Aromatase And Regulation Of Apoptosis By Aromatase Inhibitor In Cultured Endometrial Cell Of Endometriosis And Screen Endometriosis By Seldi-Tof Mass Spectrometry

BACKGROUNDEndometriosis, a benign condition in which the endometrial glands and stroma are present outside the uterine cavity. It is a common disease, which affects between 5 and 15% of 'normal' women. It is a destructive disease, and benign only in its classification as having no abnormal meiotic activity. In many other respects, it is a "malignant" disease that causes considerable anatomical destruction and symptomatology, particularly pain. Endometriosis is thought to be a polygenically inherited disease with a complex, multifactorial etiology. Moreover, it is an estrogen-dependent disorder that tends to regress after estrogen deprivation. Aromatase, also called estrogen synthetase, catalyzes aromatization of androgens to estrogens and is a key enzyme in estrogen biosynthesis. The expression of aromatase has been identified in endometriotic tissue and in the endometrium of women with endometriosis and in the stroma of endometriotic and in adenomyotic tissue. For this reason and because treatment is desired to act locally on the lesions rather than to block ovarian function, use of two new types of drugs to inhibit estrogen action has been proposed: the aromatase inhibitors, and the selective estrogen receptor modulator (SERM) raloxifene.OBJECTIVES1. To establish the primary co-cultured cell models of endometrial stromal cells and endometrial epithelial cells from endometriosis and non-endometriosis patients and the primary subepithelial stromal cell models of endometriotic implants. The spontaneous apoptosis in these cultured cells were evaluated. 2. To investigate the expression of aromatase and its transcription regulators—Steroidogenic Factor-1 (SF-1) and Chicken Ovalbumin Upstream Promoter Transcription Factor (COUP-TF) in three groups of primary cultured cells in vitro. 3. To determine the effects of estradiol, the aromatase inhibitors and the selective estrogen receptor modulators (SERM) on the expressions of aromatase, SF-1 and COUP-TF and apoptosis in these cultured cells. 4.